Bronchiolitis pathophysiology

Bronchiolitis is transmitted via air droplets. It is caused by respiratory syncytial virus (RSV), which infects the nasopharyngeal mucosa. After the infection, the virus spreads to the lower airway tracts until it reaches the bronchioles, where viral replication takes place. The viral infection induces inflammation, which leads to edema and necrosis of the bronchiolar epithelium. Cough reflex occurs due to exposure of the subepithelial tissue and nerve fibers. Vascular permeability increases, leading to edema and swelling. Histopathologically, bronchiolitis obliterans shows intraluminal polyps, inflammatory infiltration, and macrophages. Constrictive bronchiolitis shows thickening of the airways and interluminal narrowing.

• Bronchiolitis is not transmissible between individuals. However, when bronchiolitis is caused by respiratory syncytial virus (RSV), it may be transmitted via air droplets.
• Air droplets containing respiratory syncytial virus (RSV) lead to infection of the nasopharyngeal mucosa and subsequent bronchiolitis.

Bronchiolitis is caused by viral replication and inflammation as follows:^[1]

• Starting from the nasopharyngeal mucosa, respiratory syncytial virus (RSV) spreads to the lower respiratory tracts. After reaching the bronchioles, viral replication takes place.
• The respiratory syncytial virus (RSV) infection induces an inflammatory response. This leads to infiltration of inflammatory cells (RSV-specific lymphocytes), edema, and necrosis of the epithelium in the bronchioles. The epithelium is then sloughed into the lumina, causing proliferation of cuboidal epithelial cells without cilia.^[2]
• Respiratory syncytial virus (RSV) causes lysis of the epithelial tissue, which leads to the exposure of the subepithelial tissue and nerve fibers, inducing a cough reflex.
• The vascular permeability increases, which results in edema and swelling.
• This inflammatory process leads to complete or partial obstruction due to reduction in bronchiolar lumina. Accumulation of necrotic tissue produces a valve mechanism, leading to hyperinflation of the lungs.
• By this mechanism, air flow may increase into the lungs by increased negative pressure during inspiration but is unable to flow out of the lung, as the airway’s diameter is smaller during expiration.^[2] Obstructed areas may evolve into areas of atelectasis.
• In children, Kohn channels are not well developed, so atelectasis and hyperinflation may be more severe.

• There are no associated conditions with bronchiolitis.

• There are no specific findings in the gross pathology of bronchiolitis.

Bronchiolitis shows histopathological findings which vary according to different types of bronchiolitis.^[3]

• Bronchiolitis obliterans:
  • Intraluminal polyps (protrusions inside the bronchioles with fibroblastic proliferation)
  • Inflammatory infiltration
  • Type two pneumocytes lining the alveoli
  • Macrophages

• Constrictive bronchiolitis:
  • Scars leading to interluminal narrowing and obstruction
  • Thickening of the airways due to submucosal collagen and fibrosis

• Proliferative bronchiolitis:
  • Histopathology shows Masson bodies (fibrotic buds extending into alveoli)

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